The aims of this project are to: (1) localize the sites of changes in pulmonary vascular resistance in the transition from the fetal to the neonatal state, and (2) investigate the factors which may control these changes. The effects of variation in alveolar pressure on pulmonary vascular resistance in the liquid-filled lung and the air-filled lung of exteriorized fetal goats will be studied using a model involving Starling Resistors. By means of the model, changes in pulmonary vascular resistance will be segmented. Sites of postulated Starling resistors will be determined. The effects of potent vasodilators (prostaglandins of the E series) on pulmonary vascular resistance and systemic circulation will be made in the fetal and neonatal state. Analysis of the specific locus of action of several of the pulmonary vasodilators and diuretics will be made in fetus and newborn using the Starling Resistor Model. The potential significance of this research lies in the fact that it will permit segmented analysis of normal and abnormal pulmonary circulation in the fetus and newborn. Knowledge of specific sites of pulmonary vascular resistance and factors which control this resistance (including drugs) should be of use in a rational approach to therapy of respiratory distress. BIBLIOGRAPHIC REFERENCES: Cassin, S., Tyler, T., and Wallis, R., The Effects of Prostaglandin E1 on Foetal Pulmonary Vascular Resistance. Proc. Soc. Exper. Biol. & Med. 148:584-587, 1975. Cassin, S., Tyler, T., and R. Wallis. Prostaglandin E1 and Foetal Pulmonary Vascular Resistance. Clin. Res. 23:73A, 1975.